Institution
Khalifa University
Education•Abu Dhabi, United Arab Emirates•
About: Khalifa University is a education organization based out in Abu Dhabi, United Arab Emirates. It is known for research contribution in the topics: Computer science & Adsorption. The organization has 3752 authors who have published 10909 publications receiving 141629 citations.
Topics: Computer science, Adsorption, Population, Membrane, Cloud computing
Papers published on a yearly basis
Papers
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TL;DR: The COVID Human Genetic Effort established to test the general hypothesis that life-threatening COVID-19 in some or most patients may be caused by monogenic inborn errors of immunity to SARS-CoV-2 with incomplete or complete penetrance finds an enrichment in variants predicted to be loss-of-function (pLOF), with a minor allele frequency <0.001.
Abstract: Clinical outcome upon infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) ranges from silent infection to lethal coronavirus disease 2019 (COVID-19). We have found an enrichment in rare variants predicted to be loss-of-function (LOF) at the 13 human loci known to govern Toll-like receptor 3 (TLR3)- and interferon regulatory factor 7 (IRF7)-dependent type I interferon (IFN) immunity to influenza virus in 659 patients with life-threatening COVID-19 pneumonia relative to 534 subjects with asymptomatic or benign infection. By testing these and other rare variants at these 13 loci, we experimentally defined LOF variants underlying autosomal-recessive or autosomal-dominant deficiencies in 23 patients (3.5%) 17 to 77 years of age. We show that human fibroblasts with mutations affecting this circuit are vulnerable to SARS-CoV-2. Inborn errors of TLR3- and IRF7-dependent type I IFN immunity can underlie life-threatening COVID-19 pneumonia in patients with no prior severe infection.
1,659 citations
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University of Sannio1, VU University Amsterdam2, University of São Paulo3, University of California, Santa Cruz4, Harvard University5, Khalifa University6, Columbia University7, University of Texas MD Anderson Cancer Center8, Henry Ford Hospital9, Henry Ford Health System10, Baylor College of Medicine11, Memorial Sloan Kettering Cancer Center12, Emory University13, Ohio State University14, Case Western Reserve University15, University of California, San Francisco16, Princess Margaret Cancer Centre17, Van Andel Institute18, University of Washington19
TL;DR: The complete set of genes associated with 1,122 diffuse grade II-III-IV gliomas were defined from The Cancer Genome Atlas and molecular profiles were used to improve disease classification, identify molecular correlations, and provide insights into the progression from low- to high-grade disease.
1,535 citations
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03 May 2017TL;DR: This work used a crowd-sourced hate speech lexicon to collect tweets containing hate speech keywords and labels a sample of these tweets into three categories: those containinghate speech, only offensive language, and those with neither.
Abstract: A key challenge for automatic hate-speech detection on social media is the separation of hate speech from other instances of offensive language. Lexical detection methods tend to have low precision because they classify all messages containing particular terms as hate speech and previous work using supervised learning has failed to distinguish between the two categories. We used a crowd-sourced hate speech lexicon to collect tweets containing hate speech keywords. We use crowd-sourcing to label a sample of these tweets into three categories: those containing hate speech, only offensive language, and those with neither. We train a multi-class classifier to distinguish between these different categories. Close analysis of the predictions and the errors shows when we can reliably separate hate speech from other offensive language and when this differentiation is more difficult. We find that racist and homophobic tweets are more likely to be classified as hate speech but that sexist tweets are generally classified as offensive. Tweets without explicit hate keywords are also more difficult to classify.
1,425 citations
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TL;DR: Different predictive biomarkers for anti-PD-1/PD-L1 and anti-CTLA-4 inhibitors, including immune cells, PD-L 1 overexpression, neoantigens, and genetic and epigenetic signatures are discussed, which could improve the efficacy of this promising new cancer therapy.
Abstract: Cancer growth and progression are associated with immune suppression. Cancer cells have the ability to activate different immune checkpoint pathways that harbor immunosuppressive functions. Monoclonal antibodies that target immune checkpoints provided an immense breakthrough in cancer therapeutics. Among the immune checkpoint inhibitors, PD-1/PD-L1 and CTLA-4 inhibitors showed promising therapeutic outcomes, and some have been approved for certain cancer treatments, while others are under clinical trials. Recent reports have shown that patients with various malignancies benefit from immune checkpoint inhibitor treatment. However, mainstream initiation of immune checkpoint therapy to treat cancers is obstructed by the low response rate and immune-related adverse events in some cancer patients. This has given rise to the need for developing sets of biomarkers that predict the response to immune checkpoint blockade and immune-related adverse events. In this review, we discuss different predictive biomarkers for anti-PD-1/PD-L1 and anti-CTLA-4 inhibitors, including immune cells, PD-L1 overexpression, neoantigens, and genetic and epigenetic signatures. Potential approaches for further developing highly reliable predictive biomarkers should facilitate patient selection for and decision-making related to immune checkpoint inhibitor-based therapies.
1,296 citations
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TL;DR: In this article, the use of carbon nanotubes (CNTs), member of the fullerene structural family, is considered with special focus on the removal of heavy metals from water (lead, chromium, cadmium, arsenic, copper, zinc and nickel).
946 citations
Authors
Showing all 3860 results
Name | H-index | Papers | Citations |
---|---|---|---|
Xavier Estivill | 110 | 673 | 59568 |
Gordon McKay | 97 | 661 | 61390 |
Muhammad Imran | 94 | 3053 | 51728 |
Muhammad Shahbaz | 92 | 1001 | 34170 |
Paul J. Thornalley | 89 | 321 | 27613 |
Paolo Dario | 86 | 1034 | 31541 |
N. Vilchez | 83 | 133 | 25834 |
Andrew Jones | 83 | 695 | 28290 |
Christophe Ballif | 82 | 696 | 26162 |
Khaled Ben Letaief | 79 | 774 | 29387 |
Muhammad Iqbal | 77 | 961 | 23821 |
George K. Karagiannidis | 76 | 653 | 24066 |
Hilal A. Lashuel | 73 | 233 | 18485 |
Nasir Memon | 73 | 392 | 19189 |
Nidal Hilal | 72 | 395 | 21524 |